Mechanisms of head-shaking nystagmus (HSN) require further exploration in central vestibular disorders. To determine whether impaired uvulonodular inhibition over the velocity storage of the vestibulo-ocular reflex (VOR) is the mechanism of ipsilesional HSN in lateral medullary infarction (LMI), 17 patients with ipsilesional HSN and LMI underwent measurements of the VOR gains during low-frequency sinusoidal harmonic accelerations, and the time constants (TC) of the VOR and tilt suppression of the post-otatory nystagmus during step-velocity rotation. Compared with normal controls, the patients showed increased VOR gains without difference between ipsi- and contralesional rotations, while the VOR TCs were decreased without directional asymmetry during step-velocity rotation. In contrast, the patients showed impaired tilt suppression of the postrotatory nystagmus, and the impairment of tilt suppression was more severe after contralesional than ipsilesional rotation. The asymmetric tilt suppression may generate ipsilesional HSN by increasing contralesional velocity storage during head shaking, and may be ascribed to disruption of ipsilesional nodulo-uvular inhibition of the velocity storage mechanism.